diindolylmethane

anyone familiar with diindolylmethane ???

i know that it's a popular supplement for menopausal women but a bro of mine was saying that guys can use it as an aromatose inhibitor... i tried to find some detail to support or debunk his claim but can't seem to find anything that provides any data on how this stuff works... i can't imagine that it would be poplular with the menopausal crowd if it caused even lower estrogen in any way so just looking to see if anyone here as any info on this stuff and what it actually does...

thanks
~dim

never heard of it....bump

DIM is not an aromatase inhibitor but is an estrogen imitator-blocker that has subtle but definite bloat and gyno preventitive effects, If you read my advise on pct I made reference to it as one I personally use but most bbers do not like it.

thanks Bear...

i will try to search for your pct post and read it (again, no doubt)... thanks again for sharing your knowledge...

btw, I did search for diindolylmethane before posting this question and returned nothing...

funny that diindolylmethane is commonly called DIM, but that has nothing to do with my screen name... ok maybe it's not funny... damn, i think i need more coffee...

thanks again Bear...

~dim

try dim antiestrogen as search words
Beyond-a-century.com carries it but their information is often erroneous. They still promote chrysin as an antiestrogen but chrysin is blocked by the body as soon as it is digested.


some examples:
http://www.lef.org/magazine/mag2004/jan2004_report_cancer_02.htm
http://sites.browsermanaged.com/folder8175/estronex.pdf

http://www.integratedhealth.com/infoabstract/i3cab.html
DIM is a weak agonist for the aryl hydrocarbon (Ah) receptor and blocks the effects of estrogens via inhibitory Ah receptor-estrogen receptor cross-talk. DIM and various structural analogs were examined in H295R cells for effects on 3 cytochrome P450 (CYP) enzymes involved in estrogen synthesis and/or metabolism: CYP1A1, CYP1B1, and CYP19 (aromatase). Aromatase activity was measured by conversion of 1 beta-(3)H- androstenedione to estrone and (3)H(2)O. H295R cells were exposed to the test chemicals dissolved in dimethyl sulfoxide for 24 h prior to analyses. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) (0--30 nM) and DIM (0--10 microM) induced ethoxyresorufin-O-deethylase (EROD) activity, as a measure of CYP1A1 and possibly 1B1 activity, with EC(50) values of about 0.3 nM and 3 microM, respectively. DIM, but not TCDD, induced aromatase activity with an apparently maximal 2- fold increase at 10 microM; higher concentrations of DIM and many of its analogs were cytotoxic. TCDD (30 nM) significantly increased CYP1A1 and 1B1 mRNA levels, but had no effect on mRNA for CYP19. DIM (3 microM) significantly increased mRNA levels for all three CYPS: DIM analogs with substitutions on the 5 and 5' position (3 microM) induced aromatase and EROD activity, together with mRNA levels of CYP1A1, 1B1, and 19; analogs that were substituted on the central carbon of the methane group showed little or no inductive activity toward the CYPS: In conclusion, DIM and several of its analogs appear to induce CYPs via multiple yet distinct pathways in H295R human adrenocortical carcinoma cells.